Predisposition to the development of IL-9-secreting T cells in atopic infants.
作者信息
Yao Weiguo, Tepper Robert S, Kaplan Mark H
出版信息
J Allergy Clin Immunol. 2011 Dec;128(6):1357-1360.e5. doi: 10.1016/j.jaci.2011.06.019. Epub 2011 Jul 28.
Abstract
摘要
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本文引用的文献
1
A brief history of IL-9.白细胞介素-9 的简史。
J Immunol. 2011 Mar 15;186(6):3283-8. doi: 10.4049/jimmunol.1003049.
2
Evaluation of airway reactivity and immune characteristics as risk factors for wheezing early in life.评估气道反应性和免疫特征作为生命早期喘息的危险因素。
J Allergy Clin Immunol. 2010 Sep;126(3):483-8.e1. doi: 10.1016/j.jaci.2010.06.028.
3
The transcription factor PU.1 is required for the development of IL-9-producing T cells and allergic inflammation.转录因子 PU.1 是产生白细胞介素 9 的 T 细胞和过敏炎症发育所必需的。
Nat Immunol. 2010 Jun;11(6):527-34. doi: 10.1038/ni.1867. Epub 2010 May 2.
4
IL-4 inhibits TGF-beta-induced Foxp3+ T cells and, together with TGF-beta, generates IL-9+ IL-10+ Foxp3(-) effector T cells.白细胞介素-4抑制转化生长因子-β诱导的叉头框蛋白3阳性T细胞，并与转化生长因子-β共同产生白细胞介素-9阳性、白细胞介素-10阳性、叉头框蛋白3阴性效应T细胞。
Nat Immunol. 2008 Dec;9(12):1347-55. doi: 10.1038/ni.1677. Epub 2008 Nov 9.
5
Transforming growth factor-beta 'reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset.转化生长因子-β“重编程”辅助性T细胞2的分化并促进产生白细胞介素9的亚群。
Nat Immunol. 2008 Dec;9(12):1341-6. doi: 10.1038/ni.1659. Epub 2008 Oct 19.
6
Expired nitric oxide and airway reactivity in infants at risk for asthma.哮喘高危婴儿的呼出一氧化氮与气道反应性
J Allergy Clin Immunol. 2008 Oct;122(4):760-765. doi: 10.1016/j.jaci.2008.07.022. Epub 2008 Aug 28.
7
Allergen-induced interleukin-9 production in vitro: correlation with atopy in human adults and comparison with interleukin-5 and interleukin-13.变应原诱导的白细胞介素-9体外产生：与成年人类特应性的相关性及与白细胞介素-5和白细胞介素-13的比较
Clin Exp Allergy. 2006 Feb;36(2):174-82. doi: 10.1111/j.1365-2222.2006.02422.x.
8
9
Allergen-induced Th1 and Th2 cytokine secretion in relation to specific allergen sensitization and atopic symptoms in children.变应原诱导的儿童Th1和Th2细胞因子分泌与特异性变应原致敏及特应性症状的关系
Clin Exp Allergy. 2001 Oct;31(10):1528-35. doi: 10.1046/j.1365-2222.2001.01190.x.
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